Neuroprotective Effects of Peanut Skin Extract Against Oxidative Injury in HT-22 Neuronal Cells

Area of Science:

• Neuroscience
• Biochemistry
• Pharmacology

Background:

• Oxidative stress is a critical factor in neurological disorders.
• Peanut skins, a byproduct of the peanut industry, are rich in antioxidants and show potential for neuroprotection.

Purpose of the Study:

• To investigate the neuroprotective effects of peanut skin extract (PSE) against oxidative injury in HT-22 neuronal cells.
• To elucidate the underlying mechanisms of PSE's neuroprotective action.

Main Methods:

• Preparation of peanut skin extract (PSE) and quantification of its phenolic compounds.
• Assessment of PSE's radical scavenging activity.
• Evaluation of PSE's protective effects against tert-butyl hydroperoxide (t-BHP)-induced oxidative stress in HT-22 cells, including measurements of reactive oxygen species (ROS), lipid peroxidation, mitochondrial function, and apoptosis.
• Mechanistic studies using network pharmacology and experimental validation of the PI3K/Akt/Nrf2 signaling pathway.

Main Results:

• PSE is rich in phenolic compounds and exhibits potent antioxidant activity.
• PSE pretreatment significantly reduced ROS generation and lipid peroxidation, enhanced endogenous antioxidants (SOD, GSH/GSSG ratio), preserved mitochondrial membrane potential, inhibited cytochrome c release, and prevented apoptosis in t-BHP-treated HT-22 cells.
• The neuroprotective effects of PSE were comparable to edaravone and mediated by the PI3K/Akt/Nrf2 signaling pathway, leading to upregulation of Nrf2 and its downstream antioxidant proteins (HO-1, NQO1).

Conclusions:

• Peanut skin extract demonstrates significant neuroprotective properties against oxidative stress-induced neuronal damage.
• PSE acts by restoring oxidative balance, protecting mitochondria, and inhibiting apoptosis, primarily through the PI3K/Akt/Nrf2 pathway.
• PSE holds promise as a natural therapeutic agent for oxidative-related neurological disorders.